Janna L. Harris1, Henry Yeh2,
Nancy E. Berman3, William M. Brooks1
1Hoglund Brain Imaging Center,
University of Kansas Medical Center, Kansas City, KS, United States; 2Department
of Biostatistics, University of Kansas Medical Center, Kansas City, KS, United
States; 3Department of Anatomy & Cell Biology, University of
Kansas Medical Center, Kansas City, KS, United States
N-acetylaspartate
(NAA), a metabolite synthesized in neuronal mitochondria and detected by
proton magnetic resonance spectroscopy (MRS), might serve as a non-invasive
biomarker of mitochondrial integrity after traumatic brain injury (TBI).
Previous studies in human survivors of TBI have linked NAA with cognitive
recovery, although the specific mechanism has not been elucidated. We have examined
a time course of changes in NAA and behavioral impairment after TBI in a
well-characterized animal model. We then investigated whether these NAA
changes are sensitive to manipulation of mitochondrial status by cyclosporine
A (CsA), an experimental neuroprotective agent that inhibits mitochondrial
permeability transition after TBI.
Keywords